Dietary fatty acid determines the intestinal absorption of lutein in lutein deficient mice

- Components and size of mixed micelles in the intestine influence lutein absorption.
- Fatty acids have the potential to enhance the intestinal uptake of lutein.
- Olive and coconut oils improve the intestinal absorption of lutein in mice.

The present investigation was undertaken to study the influence of dietary lipids [olive (OO), coconut (CNO), groundnut (GNO), soybean (SBO), sunflower (SFO), rice bran (RBO), corn (CO), palm (PO), fish (FO) oils] on the bioavailability and antioxidant property of lutein in lutein deficient (LD) mice. Lutein (200 μM) was dispersed in dietary lipids and administered to LD mice for a period of 15 days. The plasma lutein levels were found to be highest in OO (82%) and CNO (68%), when compared to the control (mixed micelle) group. Further, positive correlation was found between intestinal triacylglycerol lipase and plasma lutein levels, confirming the crucial role of intestinal lipase on lutein micellarization and its intestinal uptake. Results revealed an affirmative correlation between triglycerides, low density lipoproteins and high density lipoprotein levels with plasma and tissue lutein levels, signifying their role in the transportation of newly absorbed lutein to target tissues. Furthermore, lutein accumulation in the liver and the eye was highest in the OO (120% and 117%) and CNO (105% and 109%) fed groups, compared to control. Lutein deficiency resulted in elevated (p < 0.05) levels of lipid peroxides, superoxide dismutase, and catalase in plasma and liver microsomes, which have been decreased significantly on feeding lutein. These results may be due to the influence of oleic (dominant in OO) and lauric (dominant in CNO) acids on the activity of intestinal lipase, portal absorption, triglycerides, lipoprotein or cholesterol flux between liver and peripheral tissues, which may modulate the uptake and transport of lutein.